10.1161/CIRCULATIONAHA.116.024471 1 Catheter Ablation of Atypical Atrioventricular Nodal Reentrant Tachycardia Running Title: Katritsis et al.;Atypical AVNRT Ablation Demosthenes G. Katritsis, MD, PhD 1,2 ; Joseph E. Marine, MD 3 ; Fernando M. Contreras, MD 1 ; Akira Fujii, MD 4 ; Rakesh Latchamsetty, MD 5 ; Konstantinos C. Siontis, MD 5 ; George D. Katritsis, MBChB, BSc 6 ; Theodoros Zografos, MD 2 ; Roy M. John, MD 4 ; Lawrence M. Epstein, MD 4 ; Gregory F. Michaud, MD 4 ; Elad Anter, MD 1 ; Ali Sepahpour, MD 7 ; Edward Rowland, MD 7 ; Alfred E. Buxton, MD 1 ; Hugh Calkins, MD 3 ; Fred Morady, MD, 5 William G. Stevenson, MD 4 ; Mark E. Josephson, MD 1 1 Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA; 2 Athens Euroclinic, Athens, Greece; 3 Johns Hopkins Hospital, Baltimore, MD; 4 Brigham and Women’s Hospital, Harvard Medical School, Boston, MA; 5 University of Michigan Health System, Ann Arbor, MI; 6 The Oxford University Clinical Academic Graduate School, Oxford, UK; 7 The Heart Hospital, London, UK Address for Correspondence: Dr. D. Katritsis Division of Cardiology Beth Israel Deaconess Medical Center 185 Pilgrim Rd, Baker 4 Boston, MA 02215 Tel: +306944845505 Fax: +302106416535 Email: [email protected]or [email protected]Journal Subject Terms: Arrhythmias 1 Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA MA ; ; ; 2 At At Athe he hens ns ns Euroclinic, Athens, Greece ; 3 Johns Hopki ns Hospital, Baltimore, MD ; 4 Brigham and Women’s Hospital, Harvard Medical School, Boston, MA; 5 University of Michigan Health System, Ann Ar Ar Arbo bo bor r r, M M MI; 6 6 T The Oxford University Clinical A Academic Grad dua u te S School, Oxford, UK ; 7 7 7 Th Th The e e He Heart Ho ospit ta al, Lo Lo Lond ndon on n, , UK UK K A dd d dre re ress ss ss for or r C C Corre resp pondenc nc nce: e: e Dr . D . Ka K tritsis
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10.1161/CIRCULATIONAHA.116.024471
1
Catheter Ablation of Atypical Atrioventricular
Nodal Reentrant Tachycardia
Running Title: Katritsis et al.;Atypical AVNRT Ablation
Demosthenes G. Katritsis, MD, PhD1,2; Joseph E. Marine, MD3; Fernando M. Contreras, MD1;
Akira Fujii, MD4; Rakesh Latchamsetty, MD5; Konstantinos C. Siontis, MD5;
George D. Katritsis, MBChB, BSc6; Theodoros Zografos, MD2; Roy M. John, MD4;
Lawrence M. Epstein, MD4; Gregory F. Michaud, MD4; Elad Anter, MD1; Ali Sepahpour, MD7;
Edward Rowland, MD7; Alfred E. Buxton, MD1; Hugh Calkins, MD3; Fred Morady, MD,5
William G. Stevenson, MD4; Mark E. Josephson, MD1
1Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA; 2Athens
Hospital, Harvard Medical School, Boston, MA;5University of Michigan Health System, Ann
Arbor, MI; 6The Oxford University Clinical Academic Graduate School, Oxford, UK;7The Heart Hospital, London, UK
Address for Correspondence: Dr. D. KatritsisDivision of Cardiology Beth Israel Deaconess Medical Center185 Pilgrim Rd, Baker 4 Boston, MA 02215 Tel: +306944845505 Fax: +302106416535 Email: [email protected] or [email protected]
Journal Subject Terms: Arrhythmias
1Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MAMA;;; 2AtAtAthehehensnsns
P=0.650), respectively. Slow pathway ablation was accomplished from the right ssepepeptutuum m m ininin 1111011
patients, and from the left septum in 3 patients, in the atypical group. There was no nneedd foff r
additional ablation lesions at other anatomical sites, and no cases of AV block were encountered
Recurrererencncee e rararates ofofof the arrhythmia were 5.6% in tthehh atypical (6/108 patatients), and 1.8% in the
ypiicacacal (2/111 papapatiiieeents)s)s gggroror upupps,s,s, iiin n n thththe nenext 3 mmmono thths fooollllllowowowinining ababblalalatitionn (P=0=0=0.1616167)7)7).
Concncnclusions— CCCononveenntn ionananall l ablation att the annaatomomicalalal aaarerereaa a oof thehe slooww papaathway isisis — thhee theraapy
of chohohoiciciceee fooorr r sysysymppttomamatic AVAVAVNRNRNRT,T,T, regggarara dlesesesss off wwheheheththt errr tttheheh tttypppicicicala oorr atttypypypici alalal fffooro mm is presesent.
10.1161/CIRCULATIONAHA.116.024471
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Clinical Perspective
What is new?
Atypical AVNRT, regardless of the type, can be successfully ablated by targeting the
anatomic area of the slow pathway.
When a right septal approach is not successful, the anatomic area of the slow pathway
can be ablated from the left septum.
Higher septal lesions that may increase the risk of inadvertent AV block or lesions
within the coronary sinus os are not necessary for the ablation of atypical AVNRT.
It seems that the same slow pathway participates in both typical and atypical AVNRT.
What are the clinical implications?
Catheter ablation at the anatomical area of the slow pathway from the right or left
septum is the treatment of choice for atypical AVNRT.
This approach is not associated with an increased risk of inadvertent AV block.
The recurrence rate following ablation of atypical AVNRT may not be significantly
higher than that seen following ablation of typical AVNRT.
It seems that the same slow pathway participates in both typical and atyypipicacal AVAVA NRNRTT.
What araree thththe cliniccala implications?
CCaC ththeterer aaablblb aatioioon n n atat ttheheh ananatomiccall arreea ooff ththhee sllslowow ppattathwhwayay fromom tthehe rrrigigght ooor r r lelel ftft
ssepptumum is the trreatmennnt t t of cchoicee ffor atatyppicical AVNVNRTT.nnn
This approach is not associated with an increased risk of inadvertent AV block.
10.1161/CIRCULATIONAHA.116.024471
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Introduction
Atrioventricular nodal re-entrant tachycardia (AVNRT), represents the most common regular
arrhythmia encountered in clinical practice.1,2 A recent randomized trial, as well as observational
studies, have provided evidence that catheter ablation is the treatment of choice for symptomatic
patients, by substantially reducing hospitalization,3 improving quality of life,4-9 and reducing
costs.9-11
Approximately 6.4% of patients with AVNRT present with delayed retrograde atrial
activation, and these arrhythmias are characterized as atypical variants.12 Due to its low
prevalence, data on atypical AVNRT, as opposed to its typical counterpart, are scarce. Atypical
AVNRT has been identified as a predictor of lower ablation success rate,13 and the optimal
method of catheter ablation is not established. Although conventional slow pathway ablation has
been reported safe and effective for atypical AVNRT,14,15 in most published series ablation was
guided by identifying the slow pathway via consideration of retrograde atrial activation or other
techniques.16-22 These approaches, however, may result in energy delivery in the mid or superior
septum; 18,19,21,22 i.e. sites that are potentially associated with an increased risk of inadvertent
atrioventricular block.20,23
We hypothesized that since the slow pathway appears to be a component of the AVNRT
circuit regardless of typical or atypical characteristics,12,24,25 conventional slow pathway ablation
as applied for typical AVNRT, should be equally safe and effective in atypical cases. We have,
therefore, studied an extensive series of atypical AVNRT cases treated with anatomical slow
pathway ablation, and compared them to sex and age-matched patients who underwent ablation
for typical AVNRT.
AVNRT has been identified as a predictor of lower ablation success rate,r 13 and thehe oooptptptimimmalalal
method of catheter ablation is not established. Although conventional slow pathway ablation has
been reported safe and effective for atypical AVNRT,14,15 in most published series ablation was
guiddeeed by idennntititifyyyininng ththhee e slsllowww pppatatathwhwhwayy via conono sidederatititiononon oooff f rer trtrogogograradee atriaaall l acacactititivavv tionono ooor r r ototothehh r
echhhnnin ques.16-222 TTThehese aapproooaaca hes, howweever, mamam y reresuuultltlt iiinn n enneergyy ddelivveeryy y iini the mmmiid orr superirior
eptum; 18,19,21221 2,222 i.e. siites that are potentiially associai ted with an increased riskk of f inadvertent
10.1161/CIRCULATIONAHA.116.024471
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Methods
Patients
Participating centers keep detailed databases of their patients subjected to catheter ablation and
these databases were searched for eligible patients. Data from adult patients with symptomatic
AVNRT, with at least one episode every 2 months, undergoing catheter ablation at Beth Israel
Deaconess Medical Center, Boston, MA, USA (2009-2015); Rhode Island Hospital, Providence,
RI, USA (1999-2001); Athens Euroclinic, Greece (2007-2015; the Heart Hospital, London, UK
(2009-2014); the Johns Hopkins Hospital, Baltimore, MD, USA (2011-2014); the University of
Michigan Health System, Ann Arbor, MI, USA (2009-2015); and the Brigham and Women’s
Hospital, Boston, MA, USA (2008-2015), were analyzed. All patients with a diagnosis of
atypical AVNRT subjected to catheter ablation were identified, and compared to age- and sex-
matched control patients with typical AVNRT. Controls were matched to atypical cases at each
participating center. We used an optimal matching algorithm to match each atypical AVNRT
case to a typical AVNRT case of the same age and sex, at each institution. When more than one
potential eligible controls were identified within an institution (same gender and age as the
atypical case), we selected the typical AVNRT control with procedure date closest to the atypical
AVNRT case. We did not specify a priori a matching caliper width for age, because we
anticipated that exact or nearly exact matches could be identified for each atypical AVNRT case.
Patients displaying characteristics of co-existent typical and atypical AVNRT were included in
the study, but patients with other arrhythmias such as atrial flutter or fibrillation that required
additional ablation were excluded. Patients who had been subjected to ablation for AVNRT in
the past were also excluded. Electrograms and ablation characteristics of patients were studied by
authors at participating institutes and, if needed, verified by the first and last author of this report.
Hospital, Boston, MA, USA (2008-2015), were analyzed. All patients with a diaggnonoosisisis s ofofof
atypical AVNRT subjected to catheter ablation were identified, and compared to age- and sex-
matched control patients with typical AVNRT. Controls were matched to atypical cases at each
partticiccipating ceceennntererer. WeWeWe uuusesed d d ananan opopoptitt mamal l matccchihh ngg algggorororititithmhmhm to o mamamatctch eae chhh aaatytytypipipicacc l AVAVAVNRNRNRTT T
caseee ttto a typicaaal l l AVAVNRNRT caaasses of the saamme ageee aandd sexexex,, atatat eacach innsstituttioonn.n WWWhen momom rre than onone
potential eligible controls were identified d wiithin an institution (same gender and age as the
10.1161/CIRCULATIONAHA.116.024471
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All patients were studied in the post-absorptive state, under mild sedation, and after all
antiarrhythmic agents had been discontinued for more than 5 half-lives. No patient had received
amiodarone for the preceding three months. The study received approval from our institutional
review boards.
Definitions
AVNRT was diagnosed by fulfillment of established criteria during detailed atrial and
ventricular pacing maneuvers.26 Typical (slow-fast) AVNRT was defined by an atrial-His/His-
atrial ratio (AH/HA) >1, and HA interval 70 ms. Atypical AVNRT was defined by delayed
retrograde atrial activation with HA>70 ms. If the AH was <200 msec and the AH<HA, the
atypical form was characterized as fast-slow. If AH>200 ms and AH>HA, the atypical form was
considered slow-slow. Tachycardias with a prolonged AH interval >200 ms but AH<HA, or with
AH<200 ms and AH>HA, or with variable intervals during the same or different episodes, were
classified as indeterminate. Details of our methodology for measurements of intervals during
tachycardia have been described elsewhere.12,25
Mapping and Ablation
Anatomical slow pathway ablation was performed at each center according to standard
techniques.27-29 In brief, a conventional 4-mm ablation catheter was positioned at the inferior
(posterior) part of the tricuspid annulus until an A/V ratio of <1 was recorded, and the atrial
electrogram was delayed relatively to the atrial electrogram recorded at the His bundle. Care was
taken to keep the ablation catheter below the ostium of the coronary sinus (CS) as visualized in
the right anterior oblique (RAO) projection; mapping was not performed at the mid or anterior
septum (Figure 1). When multicomponent signals or separate, low-amplitude potentials were
obtained, radiofrequency (RF) current, 20-40W aimed at a temperature of 60oC, was delivered
atypical form was characterized as fast-slow. If AH>200 ms and AH>HA, the atyypipiicacacal l fofoformrmrm wwwas
considered slow-slow. Tachycardias with a prolonged AH interval >200 ms a but AH<HA, or with
AH<200 ms and AH>HA, or with variable intervals during the same or different episodes, were
classsisiified as innndddeteeermrr inininatatatee.e DeDeDetatatailillsss ofoo oouru methohohodoollogygygy fffororor mmmeaasusuurerer mementn s ofofof iiintntntererervav lsss dddurururinining g g
achhhyycy ardia haaaveveve bbeeenn ddescririribebb d elsewhwhere.12,2255
Mapping and Ablation
10.1161/CIRCULATIONAHA.116.024471
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for up to 30 sec until a junctional rhythm with 1:1 retrograde ventriculo-atrial (VA) conduction
was elicited. If VA conduction was not seen, RF delivery was immediately stopped. Once
junctional rhythm with VA conduction was recorded, energy delivery was continued for 10-30
sec or until cessation of the junctional rhythm. Following ablation, arrhythmia induction with the
use of isoproterenol was attempted. End-points for ablation success were demonstration of RF-
induced junctional rhythm conducted to the atria, and non-inducibility of AVNRT with
programmed stimulation during isoproterenol challenge.
If RF-induction of junctional rhythm or non-inducibility of tachycardia could not be
accomplished from the right side of the septum, mapping at the corresponding part of the left
septum was undertaken. In some centers, additional lesions higher in the septum or in the roof of
the proximal coronary sinus were delivered before proceeding to left septal ablation. A mapping
electrode was retrogradely introduced through the noncoronary cusp of the aortic valve to record
a left-sided His bundle electrogram as described elsewhere.30,31 Since positioning of the left
septal catheter retrogradely through the non-coronary cusp inevitably results in mapping of the
anterior part of the septum, a trans-septal approach was used for introduction of the left-sided
ablation catheter and additional mapping of the posterior part of the septum (Figure 2). Mapping
of the inferior (posterior) part of the mitral annulus, below the left-sided His was performed with
the same principles as on the right septum. At the successful ablation site the atrial electrogram is
closer to this recorded by the CS rather than the His electrode. Thus, inadvertent AV block is
avoided following ablation either from the right or the left septum.29 Following successful
ablation, patients were discharged from hospital within 24 hours on aspirin and no
antiarrhythmic drugs. All patients were followed-up for an at least 3-month interval, and
repeated ablation was performed in case of recurrence of symptoms during that time. Patients
eptum was undertaken. In some centers, additional lesions higher in the septum oror iiinn n ththhe e rororoofofof of
he proximal coronary sinus were delivered before proceeding to left septal ablation. A mapping
electrode was retrogradely introduced through the noncoronary cusp of the aortic valve to record
a leeftftt-sided Hisiss bbbununundle e e eleleleeectc rooogrgrgramamam as dedescribeeed dd eelssewhwhwherere e.e.e.3033 ,31 SSiS ncncn e e popositiiionononinining g g ofo thehehe lllefefeft t t
eptpttalala catheter r reeretrroogrraddely thhrh ough thee nnon-cororo onnaary y y cucucuspsps iinenevittabbly reresuuulttts in mapapappiinng of thhee
anterior part of the septum, a trans-septal l approachh was used for introduction of the leftf -sidedd
10.1161/CIRCULATIONAHA.116.024471
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with a diagnosis of AVNRT at repeat ablation, or patients who presented with a documented
tachycardia similar to the clinical one before ablation, were registered as failures.
Statistical analysis
Continuous, normally distributed variables are presented as mean ± standard deviation. Data
normality was analysed using the Kolmogorov-Smirnov test. In all cases the examined variables
followed the normal distribution and the Student’s t-test was used to analyse differences between
two groups, and the one-way ANOVA test to analyse differences between more than two groups.
Categorical data are expressed as frequencies (percentages) and were compared using Fisher's
exact test. All reported p-values were based on two-sided tests and were compared to a
significance level of 5%. Statistical calculations were performed on SPSS for Windows version
21 (IBM Corporation, Armonk, New York). A post hoc power analysis was performed to
estimate the achieved statistical power for the comparison of arrhythmia recurrence in the typical
and the atypical group using G*Power version 3.1.9.2 (Heinrich-Heine-Universität Düsseldorf,
Düsseldorf, Germany).32 Considering an alpha level of 0.05, and according to the sample size
used in the study and the observed difference, the present study achieved a power of 0.25. A total
sample size of 815 patients would be needed to achieve a power of 0.80 (Online appendix,
Figure 1). In exploratory analysis, the critical recurrence rate in the atypical group that the study
would be able to detect with a power of 0.80, was estimated to be 12.3% (Online appendix,
Figure 2).
ignificance level of 5%. Statistical calculations were performed on SPSS for Windnddowowows s s veveversrsrsioioionn
21 (IBM Corporation, Armonk, New York). A post hoc power analysis was performed to
estimate the achieved statistical power for the comparison of arrhythmia recurrence in the typical
and d thththe atypicalalal grororouppp uuusisisingngn GGG*P*P*Powowower vversionnn 333.11.99.2 (((HeHeHeinininrirr chh-HeHeH ini ee-U- niiiveveversrsrsitititätää Düsüsüsseseseldldldorororf,
Düssssssele dorf, Geeermrmr anany)).332 Cooonnsn idering g anan alphaaa llevveel ooof f f 0.00 05050 , aand aaccordrdinnng g g to the sssamampple sizee
used in the study and thhe observedd difference, thhe present study achievedd a power of 0.0 25. A tota
10.1161/CIRCULATIONAHA.116.024471
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Results
Patients
In total, 2079 patients with AVNRT were studied at Beth Israel Deaconess Medical Center
(Boston, MA, USA), and Rhode Island Hospital (Providence, RI, USA) (n=287); Athens
Euroclinic, Greece (n=307); the Heart Hospital, London, UK (n=179); the Johns Hopkins
Hospital, Baltimore, MD, USA (n=271); the University of Michigan Health System, Ann Arbor,
MI, USA (n=621); and the Brigham and Women’s Hospital, Boston, MA, USA (n=414). Using
the criteria mentioned above, 113 patients (5.4%) had atypical AVNRT or co-existent atypical
and typical AVNRT and no other concomitant arrhythmia. The mean age of patients with
atypical AVNRT was 48.5±18.1 years (range 14 to79), and 68 patients (60%) were female. The
control group consisted of 113 patients with typical AVNRT, age- (48.6±17.3 years) and sex-
matched to the atypical AVNRT patients, on a one-to-one basis.
Electrophysiologic characteristics
Eighty-five out of the 113 patients (75.2%) had fast-slow AVNRT according to both the AH<HA
and AH<200 ms, and 14 patients (12.4%) slow-slow AVNRT. The remaining 14 patients (12.4
%) could not be reliably classified due to inconsistent AH and HA/AH patterns or variable
intervals. There were no significant differences in age and gender among the different atypical
AVNRT forms (P = 0.592, and P = 0.323, respectively). Twenty patients (8.9%) had co-existent
typical and atypical AVNRT during the electrophysiology study. Details of this group have been
presented elsewhere.25 Atypical AVNRT was induced by ventricular pacing or extrasystoles in
27 patients (Figure 3), or spontaneously during isoprenaline infusion in 11 patients. In the
remainder atypical AVNRT was induced by high right atrial (HRA) or CS pacing (Figures 4 and
5), and in 2 of them following an anterograde conduction jump (Figure 6). In 7 out of 98
atypical AVNRT was 48.5±18.1 years (range 14 to79), and 68 patients (60%) wereree fefefemamamalelele. ThThThe
control group consisted of 113 patients with typical AVNRT, age- (48.6±17.3 years) and sex-
matched to the atypical AVNRT patients, on a one-to-one basis.
ighhht tt septal ablalalatitt onon. LeLeft sepepeptal ablationon was nnneeededed fofoforrr ononlylly onee oof thhee 77 7 ppap tients inn whw om
earliest retrograde atriial activation was recordedd bby the His electrode. Flluoroscopy and d RF times
10.1161/CIRCULATIONAHA.116.024471
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type, and one a slow-slow tachycardia. One patient had been subjected to both right and left
septal ablation. Repeat ablation was performed in 3 patients. In two of them right septal ablation
at the area of the slow pathway was unsuccessful, and a left-sided procedure, as previously
described, was necessary. Three patients refused repeated ablation and were treated with
medication. In the typical group, two patients were lost to follow-up, and recurrence was seen in
2 (1.8%) patients (P=0.167, for the percentages of recurrences in atypical vs typical AVNRT
ablation). No case of AV block was noted during follow-up in either the typical or the atypical
group.
Discussion
Our study represents the largest series of atypical AVNRT cases published. Results indicate that
conventional slow pathway ablation is generally a safe and effective method of ablation for
patients with AVNRT, regardless of the type. No cases of AV block were encountered, and
success and recurrence rates were similar for typical and atypical AVNRT ablation. We did not
find atypical AVNRT to be associated with a significantly higher rate of ablation failure, as
previously reported,5 and no significant difference in recurrence rates was detected between the
two groups, but the modest statistical power achieved in our study does not preclude the
possibility of a type II error. Anatomical slow pathway ablation, as described in our study, can be
accomplished without the need for additional pacing and other manoeuvers,33,34 and offers a safe
therapeutic approach for the management of these patients. In our extensive series, detailed
mapping and/or ablation attempts at the CS os or higher in the septal area were not necessary for
the elimination of this arrhythmia.
These results are in keeping with our previous observations that atypical AVNRT can be
induced by both atrial and ventricular extra-stimulation, and, rarely, may also be induced
Our study represents the largest series of atypical AVNRT cases published. Resulltstss iiindndndicicicatatate e thththat
conventional slow pathway ablation is generally a safe and effective method of ablation for
patients with AVNRT, regardless of the type. No cases of AV block were encountered, and
uccceeess and recucucurrrrenee ceee rrratatatese wwwererere e e sisisimiilalar for tytyt picacal annnd d d atatatypypypiccalall AAAVNVNRTR aaablblblatatatioioionn. WeWeWe dddididid nnnot
finddd aaatypical AVAVAVNRNRT to be aasa sociated wwith a sssiignnifficacaantntntlylyly hhhigiigherr rrate ooff ababablation fffaiailuurre, as
previously reported,d 55 and no signifif cant ddifference ini recurrence rates was detected between theh
10.1161/CIRCULATIONAHA.116.024471
12
following an anterograde conduction jump.12,25 The coexistence of both typical and atypical
types in the same patient, as well as the fact that spontaneous conversions from one type to
another may occur, also argue in favor of the concept that atypical and typical AVNRT may
share a common electrophysiological substrate. Although atypical AVNRT of the fast-slow type,
and typical AVNRT do not utilize the same limb for fast pathway conduction, in anatomical
models the arrhythmia circuit utilizes the same “slow” component that is most likely located in
the area of the posterior nodal extensions.35 Indeed, although there is much uncertainty about the
nature of the fast pathway, the evidence supporting the inferior nodal extensions as the anatomic
substrate of the slow pathway is strong.12,25 It was initially proposed that “fast-slow” AVNRT
utilises a posterior extension as the “slow” pathway, while the “fast” component comprised the
fast pathway of the typical form in the opposite direction,35 but this was refuted by subsequent
evidence.25 It seems more likely that all subforms of atypical AVNRT utilize the right and left
inferior extensions as the substrate of both components of their circuit (Figure 7).12 In this
context, both typical and atypical AVNRT, can be ablated by targeting the area of the slow
pathway either from the right or the left side. However, we have not been able to identify any
electrophysiological features that may predict the need for a left septal slow pathway ablation,
either for atypical or typical AVNRT. This is also the case for our patients with recurrences
following an apparently successful procedure.
Study limitations
The main limitation of our study is the low statistical power achieved for comparison of
recurrences in the typical and atypical AVNRT groups. Although we report the largest series of
atypical AVNRT cases, due to the low recurrence rates in the typical and atypical groups, a
larger sample size would be needed to establish equal effectiveness of slow pathway ablation in
utilises a posterior extension as the “slow” pathway, while the “fast” component cocompmpmpriririsesesed dd thththee e
fast pathway of the typical form in the opposite direction,35 but this was refuted by subsequent
evidence.25 It seems more likely that all subforms of atypical AVNRT utilize the right and left
nfeeririior extensisisioono s s s as tthehehe sssubububstststrararatetete ooof boboth commmpoponnentsss ofofof tttheheheir cciirircucuc it ((FiF guguurerere 777).).).12 Innn ttthihihisss
contntnteexe t, both tytytypipp cacal anand atypypypical AVNNRRT, caaan bee aablbllatatatededed bbyy targgeetingg tthee e ara ea of thhee sslow
pathway eithher from thhe right or theh left side. HoH wever, we have not been ablel to identiify any
10.1161/CIRCULATIONAHA.116.024471
13
typical and atypical AVNRT. However, even if there is a statistically significant difference, it is
likely of small magnitude and may not be as meaningful from a clinical standpoint, especially
considering the rarity of the recurrences. Second, our results have been derived by high volume
EP laboratories, and very experienced operators. Thus, whether our data can be generalized to
lower volume centers, is not known. Third, this is a retrospective collection of cases performed
by several operators in 7 different centers that participated. Still, all successful ablations were
performed by targeting the anatomic area of the slow pathway either from the right or the left
septum. Finally, a 3-month only follow-up was available for all patients, but in our experience,
AVNRT recurrences are very unlikely after the 3 first months post-ablation.
Conclusions
Atypical AVNRT can be safely and effectively treated by conventional slow pathway ablation.
Detailed mapping during tachycardia for ablation purposes, and targeting the higher septum or
the coronary sinus ostium, do not appear necessary for the ablation therapy of the vast majority
of AVNRT, whether typical or atypical.
Disclosures
None
Conclusions
Atypical AVNRT can be safely and effectively treated by conventional slow pathway ablation.
Detailed mapping during tachycardia for ablation purposes, and targeting the higher septum or
he coooronary sinininusss ooosttiuiuium,m,m ddo o nonot t apappeearar necessssas ryry forr ttthehe aablbb attioion nn ththererapa y y ofof ththhee e vav sttt mmmajaja ororititi y
of AVAVVNRT, wwhehehethheer ttyypicalall oor atypppicaal.
10.1161/CIRCULATIONAHA.116.024471
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atypical or multiple atrioventricular node reentry tachycardias. Am Heart J. 1994;128:742-58. 15. Chen J, Anselme F, Smith TW, Zimetbaum P, Epstein LM, Papageorgiou P, Josephson ME.Standard right atrial ablation is effective for atrioventricular nodal reentry with earliest activationin the coronary sinus. J Cardiovasc Electrophysiol. 2004;15:2-7.16. Strickberger SA, Kalbfleisch SJ, Williamson B, Man KC, Vorperian V, Hummel JD,Langberg JJ, Morady F. Radiofrequency catheter ablation of atypical atrioventricular nodalreentrant tachycardia. J Cardiovasc Electrophysiol. 1993;4:526-32.17. Yu WC, Chen SA, Tai CT, Lee SH, Chiang CE, Wen ZC, Chiou CW, Ueng KC, Chen YJ,Huang JL, Chang MS. Electrophysiologic characteristics and radiofrequency catheter ablation offast-slow form atrioventricular nodal reentrant tachycardia. Am J Cardiol. 1997;79:683-6.18. Otomo K, Nagata Y, Uno K, Fujiwara H, Iesaka Y. Atypical atrioventricular nodal reentranttachycardia with eccentric coronary sinus activation: electrophysiological characteristics andessential effects of left-sided ablation inside the coronary sinus. Heart Rhythm. 2007;4:421-32.19. Otomo K, Nagata Y, Taniguchi H, Uno K, Fujiwara H, Iesaka Y. Superior type of atypicalAV nodal reentrant tachycardia: incidence, characteristics, and effect of slow pathway ablation.Pacing Clin Electrophysiol. 2008;31:998-1009.20. Suzuki A, Yoshida A, Takei A, Fukuzawa K, Kiuchi K, Tanaka S, Itoh M, Imamura K,Fujiwara R, Nakanishi T, Yamashita S, Matsumoto A, Konishi H, Ichibori H, Hirata K.Visualization of the antegrade fast and slow pathway inputs in patients with slow-fastatrioventricular nodal reentrant tachycardia. Pacing Clin Electrophysiol. 2014;37:874-83.21. Kaneko Y, Nakajima T, Irie T, Suzuki F, Ota M, Iijima T, Tamura M, Iizuka T, Tamura S,Saito A, Kurabayashi M. Successful ablation of atypical atrioventricular nodal reentranttachycardia from a noncoronary sinus of Valsalva. Int Heart J. 2014;55:84-6.22. Kaneko Y, Naito S, Okishige K, Morishima I, Tobiume T, Nakajima T, Irie T, Ota M, IijimaT, Iizuka T, Tamura M, Tamura S, Saito A, Igawa O, Kato R, Matsumoto K, Suzuki F,Kurabayashi M. Atypical Fast-Slow Atrioventricular Nodal Reentrant Tachycardia Incorporatinga "Superior" Slow Pathway: A Distinct Supraventricular Tachyarrhythmia. Circulation.2016;133:114-123.23. Chen H, Shehata M, Ma W, Xu J, Cao J, Cingolani E, Swerdlow C, Chen M, Chugh SS,Wang X. Atrioventricular block during slow pathway ablation: entirely preventable? CircArrhythm Electrophysiol. 2015;8:739-44.24. Katritsis DG, Josephson ME. Classification of electrophysiological types of atrioventricularnodal re-entrant tachycardia: a reappraisal. Europace. 2013;15:1231-40.25. Katritsis DG, Marine JE, Latchamsetty R, Zografos T, Tanawuttiwat T, Sheldon SH, BuxtonAE, Calkins H, Morady F, Josephson ME. Coexistent Types of Atrioventricular Nodal Re-Entrant Tachycardia: Implications for the Tachycardia Circuit. Circ Arrhythm Electrophysiol.2015;8:1189-93.26. Katritsis DG, Josephson ME. Differential diagnosis of regular, narrow-QRS tachycardias.Heart Rhythm. 2015;12:1667-76.27. Thakur RK, Klein GJ, Yee R, Stites HW. Junctional tachycardia: a useful marker duringradiofrequency ablation for atrioventricular node reentrant tachycardia. J Am Coll Cardiol.1993;22:1706-10.28. Kalbfleisch SJ, Strickberger SA, Williamson B, Vorperian VR, Man C, Hummel JD,Langberg JJ, Morady F. Randomized comparison of anatomic and electrogram mappingapproaches to ablation of the slow pathway of atrioventricular node reentrant tachycardia. J AmColl Cardiol. 1994;23:716-723
uj wa a , Na a s , a as a S, a su o o , o s , c bo , a a .Visualization of the antegrade fast and slow pathway inputs in patients with slow-w-fafaaststsatrioventricular nodal reentrant tachycardia. Pacing Clin Electrophysiol. 2014;37::8787874-4-838383..21. Kaneko Y, Nakajima T, Irie T, Suzuki F, Ota M, Iijima T, Tamura M, Iizuka T, Tamura S,Saito A, Kurabayashi M. Successful ablation of atypical atrioventricular nodal reentrantachycardia from a noncoronary sinus of Valsalva. Int Heart J. 2014;55:84-6.JJ
22. KKKanananekeke ooo Y,Y,Y, NNaiaitto S, Okishige K, Morishima I, TTobiume T, Naakak jimama T, Irie T, Ota M, IijimaT, IIizizzuuka T, Tamamamururu a aa M,MM TTTamamururura a a S,S,S, SSSaitoto A, Igggawa aa OO, KKKatata ooo R,RR MMatatatsusumomoto KKK,, SuSuSuzuzuzuki FFF,,Kuuurarar bayashi M. AAtyypiicacacal Faaaststst-Slow ww AtAtrrioventtriicuulaar NNNodal RRReenntrrant TTachchchyycardiiia aa Inncooorporaatatinii ga "SSSupupu erior" Slololoww PPaththway:y:: AAA Distinctt SSupravvveenttriiculululararar TaTTachchyaarrrrhythhmimiia..a Circulllaatioonn.201666;1;1;1333333:114144-1-1-1233.23. Chen H, Shehata MM, Ma W, Xu J, Cao J, Cini golani E, Swerdlow C, Chen M, Chugh SS,
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29. Hintringer F, Hartikainen J, Davies DW, Heald SC, Gill JS, Ward DE, Rowland E.Prediction of atrioventricular block during radiofrequency ablation of the slow pathway of theatrioventricular node. Circulation. 1995;92:3490-6.30. Katritsis DG, Giazitzoglou E, Zografos T, Ellenbogen KA, Camm AJ. An approachto left septal slow pathway ablation. J Interv Card Electrophysiol. 2011;30:73-9.31. Katritsis DG, Papagiannis J. Anatomically left-sided septal slow pathway ablation indextrocardia and situs inversus totalis. Europace. 2008;10:1004-5.32. Faul F, Erdfelder E, Lang AG, Buchner A. G*Power 3: A flexible statistical power analysisprogram for the social, behavioral, and biomedical sciences. Behavior Research Methods.2007;39:175-191.33. Meininger GR, Calkins H. One method to reduce heart block risk during catheter ablation ofatrioventricular nodal reentrant tachycardia. J Cardiovasc Electrophysiol. 2004;15:727-8.34. Liberman L, Hordof AJ, Pass RH. Rapid atrial pacing: a useful technique during slowpathway ablation. Pacing Clin Electrophysiol. 2007;30:221-4.35. Katritsis DG, Becker A. The atrioventricular nodal reentrant tachycardia circuit: a proposal.Heart Rhythm. 2007;4:1354-60.
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Table 1. Conduction intervals during typical and atypical AVNRT.
*: no CS measurements in 15 patients, **: no CS measurements in 10 patients.CL: tachycardia cycle length; AH: atrial to His interval during tachycardia; HA (His): His to atrium interval on the His recording electrode; HA (pCS): His to atrium interval on the proximal coronary sinus recording electrode; ERAA: earliest retrograde atrial activation.
Table 2. Ablation characteristics.
Atypical AVNRTn=113
Typical AVNRTn=113
P
Fluoroscopy time (min) 20.112.2 20.8±12.9 0.730RF delivery time (min) 5.9±5.0 5.5±4.5 0.650Junctional rhythm during RF (pts) 110 111 1.000AV block (pts) 0 3 (transient) 0.247
RF: radiofrequency.
Atypical AVNRTn=113
Typical AVNRTn=113
PPP
Fluoroscopy time (min) 20.112.2 20.8±12.9 0.00 7737 00RF delivery time (min) 5.9±5.0 5.5±4.5 0.650Junctional rhythm during RF (pts) 110 111 1.000AV blooockck (((ptptpts) 0 3 (transientnt) 0.247
RF::: rrradiofrequenccyy.
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Figure Legends
Figure 1. Electrograms at the site of successful ablation Electrograms at the site of successful
ablation recorded from the right (left panel) and left (right panel) septal ablation catheters. HRA:
high right atrium; R His: His bundle recorded by the right septal electrode; L His: His bundle
recorded by the left septal electrode; R Abl: electrograms at the successful ablation site recorded
by the right septal ablation catheter; L Abl: electrograms at the successful ablation site recorded
by the left septal ablation catheter; CS: coronary sinus; I, aVF, V1, V6: 12-lead ECG leads.
Figure 2. Slow pathway mapping. Right- and left-sided mapping of the slow pathway in the
RAO and LAO projections. The left-sided ablation electrode has been introduced through a
trans-septal approach in order to map the infero-posterior septum. RAO; right anterior oblique
projection; LAO; left anterior oblique projection; L Abl: left septal ablation catheter; R Abl: right
septal ablation catheter; His: His bundle; CS: coronary sinus; RV: right ventricle; R His: His
bundle recording from the right septum; L His: His bundle recording from the left septum
Figure 3. Induction of atypical AVNRT by ventricular pacing. A few of our atypical cases had
induction by 1 to 2 response from the A, with first A blocking in the lower node and going up a
slow pathway, then down another slow pathway (the two inferior nodal inputs?) to initiate
atypical AVNRT. An alternative explanation might be simultaneous retrograde activation of both
a fast and a slow pathway, with the latter initiating the tachycardia. However, this is rather
unlikely considering the much prolonged VA time for activation of the second A following V
Figure 2. Slow pathway mapping. Right- and left-sided mapping of the slow pathwhwwayayay iiinnn thththe e e
RAO and LAO projections. The left-sided ablation electrode has been introduced through a
rans-septal approach in order to map the infero-posterior septum. RAO; right anterior oblique
eptpttalala ablation n ccac ththeteer; Hiss:s His bundllee; CS: cccoorononarrry y y sisisinnuss; RVV: righht venenentricle; R R R HHis: His
bundle recording ffrom the right septum; L HiH s: Hisi bundle recordini g from theh left septum
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pacing compared to the VA time during tachycardia.HRA: high right atrium; His: His bundle;
CS: coronary sinus; RV: right ventricle; I, II, III, V1, V6: 12-lead ECG leads.
Figure 4. Induction of atypical AVNRT by atrial pacing. Induction of atypical, “slow-slow”
AVNRT by atrial pacing (same patient as in Figure 3).
Abbreviations as in Figure 3.
Figure 5. Induction of atypical AVNRT by atrial pacing.
Induction of the “fast-slow” form of atypical AVNRT by atrial pacing.
Abbreviations as in Figure 3.
Figure 6. Induction of atypical AVNRT following anterograde conduction jump. Induction of
atypical AVNRT following an anterograde conduction jump during proximal CS pacing. In the
left panel, a S1S2 of 300 ms produces an AH=240 ms. In the right panel, a S1S2 of 290 ms results
in anterograde conduction jump (AH=300 ms) and induces tachycardia. HRA: high right atrium;
His: His bundle; CS: coronary sinus; RV: right ventricle; I, II, III, V1, V6: 12-lead ECG leads.
Abbreviations as in Figure 3.
Figure 6. Induction of atypical AVNRT following anterograde conduction jump. Induction of
atypppicicical AVNRTRTRT fffoloo looowiwiwingngn aann n anananteteterorr grrada e condndnducttionnn jjjumumump p p duduririingngng pproroxix mamamal l l CSCSCS pppacinini g.g.g. IIIn n n thththe
eftt pppanel, a S111SSS22 ooff 30000 mss ppproduces anan AH=24242 0 mms... InInIn ttthehhe riightt ppaneel,, aa a SSS1S2 of 29292 00 mms ressuults
n anterograded condud ctioi n jump (AHA =3000 ms) andd induces tachyh cardia. HRA:A higi h riight atrium;
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Figure 7. Proposed circuit of AVNRT. During typical AVNRT (slow-fast), right- or left-sided
circuits may occur with antegrade conduction through the inferior inputs and retrograde
conduction through the superior inputs (S) or the anisotropic atrionodal transitional area (AAT).
In atypical AVNRT conduction occurs anterogradely through one of the inferior inputs, left (LI)
or right (RI) and retrogradely through the other one. Depending on the orientation of the circuit
we may record the so-called fast-slow, slow-slow or inteterminate types.